Analgesic intolerance syndrome (ais) T88.7

Author: Prof. Dr. med. Peter Altmeyer

Last updated on: 29.10.2020

Synonym(s)

Analgesic hypersensitivity; Analgesic Intolerance; ASS Intolerance Syndrome; NSAID hypersensitivity; NSR hypersensitivity

Definition
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Intolerance reaction to non-steroidal anti-inflammatory drugs (NSAIDs), probably caused by a dysbalance in the arachidonic acid metabolism. S.a.o. Urticaria, intolerance urticaria.

Etiopathogenesis
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Dysbalance in arachidonic acid metabolism. Arachidonic acid is provided by phosopholipases from the phospholipids of the cell membranes of eosinophils, mast cells and leucocytes. Via lipoxygenases and cyclooxygenases (COX) two metabolic pathways are optionally taken, some of whose products have an antagonistic effect. Prostaglandins (e.g. prostaglandin E2) are produced via the leukotriene C4 (LTC4) cyclooxygenase metabolic pathway. Peptide leukotrienes (PLT) are formed via the lipoxygenase metabolic pathway. In contrast to prostaglandins, PLT have a bronchospastic and mucous-forming effect. Patients with AIS tend to produce PLT in excess, probably due to an increased activity of LTC4 synthetase (cause: possible polymorphism of the gene sequence of LTC4 synthetase on chromosome 5q). In patients with AIS, a "shifting" (unchecked change) to the lipoxygenase metabolic pathway was described after administration of NSAIDs.

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Clinical features
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Acutely intermittent or chronically recurrent urticaria, polyposis nasi and bronchial asthma (ASA asthma, analgesic asthma).

Laboratory
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Urine: leukotriene 4 increased.

Diagnosis
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Medical history: therapy-resistant urticaria, polyposis nasi (usually multiple operations of the paranasal sinuses in the medical history), bronchial asthma).

Provocation tests by nasal, oral (see below urticaria, chronic) or bronchial provocation.

Measurement of the cysteinylleukotriene release provoked by NSAIDs in vitro using commercially available tests ( CAST). In addition, a method still undergoing clinical trials, the Analgesic Intolerance Test (AIT), can be used to assess the balance between PGE2 and leukotriene release after provocation.

Therapy
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Analgesic leave. Test with montelukast (e.g. Singulair film-coated tablets) 10 mg/day before bed rest. Adaptive deactivation (development of tolerance to analgesics, especially COX-1 inhibitors).

Literature
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Brandstätter H et al (2010) Immediate hypersensitivity reactions to nonsteroidal anti-inflammatory drugs: allergy or pseudo-allergy? Rev Med Suisse 6:1345-1348 https://www.ncbi.nlm.nih.gov/pubmed/20684128
Hecksteden K et al (2003) Diagnosis of the analgesic intolerance syndrome by means of functional cell testing (Analgesic Intolerance Test: AIT). Allergology 26: 263-271
Kleine-Tebbe J et al.(2016) Food Allergy and Intolerance Distinction, Definitions and Delimitation. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz 59:705 722.
McNeil BD et al. (2015) Identification of a mast-cell-specific receptor crucial for pseudo-allergic drug reactions. Nature 519:237-241.
Pichler WJ et al (2016) Classification of Drug Hypersensitivity into Allergic, p-i, and Pseudo-Allergic Forms. Int Arch Allergy Immunol 171:166-179.
Ponvert C et al (2003) Vaccine allergy and pseudo-allergy. Eur J Dermatol 13:10-15.
Sanak M et al (1997) C4 synthetase promotor polymorphisms and risk of aspirin-induced asthma. Lancet 29: 1599-1600
Schäfer D et al (1996) Effect of prostaglandin E2 on eicosanoid release by human bronchial biopsy specimens from normal and inflamed mucosa. Chest 51: 919-923
Seitz CS et al (2014) Non-steroidal anti-inflammatory drug hypersensitivity: association with elevated basal serum trypt se? Allergy Asthma Clin Immunol 10:19.
Waller DG (2011) Allergy, pseudo-allergy and non-allergy Br J Clin Pharmacol 71:637-638.